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• W2121013171 abstract "Background Microvascular ischemia-reperfusion (I/R) injury is characterized by failure of capillary perfusion (“no-reflow”) and reoxygenation-associated phenomena (“reflow-paradox”), including activation of leukocyte-endothelium interaction with cytotoxic mediator-induced loss of endothelial integrity. The objectives of this study were to elucidate the impact of both prostaglandins E1 (PGE1) and I2 (PGI2) in microvascular reperfusion injury, with special focus on the distinct pathophysiology of no-reflow- and reflow-paradox phenomena. Materials and methods By use of the hamster dorsal skinfold preparation and in vivo fluorescence microscopy, the microcirculation of a striated skin muscle was assessed before 4 h of pressure-induced ischemia and 0.5, 2, and 24 h after onset of reperfusion. Results I/R was characterized by enhanced leukocyte-endothelium interaction in postcapillary venules, increase of macromolecular leakage, and reduction of functional capillary perfusion (P < 0.05). Intravenous 2-h infusion of PGE1, starting with onset of reperfusion, reduced leukocyte adhesion and macromolecular leakage in postcapillary venules during early reperfusion (P < 0.05), while 6-h infusion, given during ischemia and early reperfusion, showed no significant effects. PGI2 infusion also attenuated postischemic leukocyte adhesion, which was significant by a 6-h prolonged administration (P < 0.05), but did not influence the increase of microvascular permeability. Both prostaglandins were unable to prevent the postischemic failure of capillary perfusion (no-reflow). Conclusions Both prostaglandins did not significantly influence postischemic no-reflow phenomena, but appeared as potent inhibitors of reflow-paradox under the experimental circumstances of this study." @default.
• W2121013171 created "2016-06-24" @default.
• W2121013171 creator A5002090343 @default.
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• W2121013171 date "2004-07-01" @default.
• W2121013171 modified "2023-10-18" @default.
• W2121013171 title "Microvascular in vivo assessment of reperfusion injury: significance of prostaglandin E1 and I2 in postischemic “no-reflow” and “reflow-paradox”" @default.
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• W2121013171 doi "https://doi.org/10.1016/s0022-4804(03)00332-9" @default.
• W2121013171 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15172184" @default.
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